F10 and hereditary antithrombin deficiency: Finally, this duplication was also genotyped in 127cases with antithrombin deficiency carrying a genetic defect in exons or flanking regions of SERPINC1. One case, a 32-year old woman with 52% anti-FXa who developed recurrent thrombophlebitis, carried this polymorphism in combination with a three base pair deletion in exon 5(CD930907) that maintaining the reading frame caused the deletion of a glutamic acid (p.Glu344del), mutation previously described by Chowdhury and coworkers in a patient with a type I deficiency [24].